To the Editor: Baylisascaris procyonis, a roundworm parasite of
raccoons (Procyon lotor), increasingly is being documented as a cause of
severe human disease (1). Approximately 130 species of wild and
domesticated animals have been affected with B. procyonis neural larva
migrans, and the parasite is increasingly recognized as a cause of human
encephalitis (2; K. Kazacos, unpub. data). The first recognized human
case was reported in 1984 in a 10-month-old child in Pennsylvania, USA
(3). Since then, -30 additional cases of severe or fatal B. procyonis
encephalitis have been reported in the United States (4-7; K. Kazacos,
pers. comm.). To our knowledge, only 1 account of human B. procyonis
infection has been reported in Canada (in 2009) (8). We report another
case of human B. procyonis infection in Canada, indicating its probable
transmission from peridomestic raccoons.

In 2008, a 14-month-old previously healthy boy in Hamilton,
Ontario, Canada, sought care for fever, regression in speech for 5 days,
and failure to bear weight for 2 days. His parents also noticed that he
was not tracking with his eyes. Caregivers recalled a macular rash on
the face and trunk that had faded over time. The child was hospitalized,
and a workup for encephalitis was initiated. He was hemodynamically
stable and had flaccid tone, with inability to bear weight. No visible
rashes were found. A fundoscopic examination indicated no evidence of
unilateral chorioretinitis. The child was unable to track objects, which
suggested vision loss in both eyes. Blood cultures, urine cultures, and
lumbar puncture were performed. Results of blood analyses showed the
following: lymphocytes 24% (45%76%), monocytes 41% (3%-6%), eosinophils
32% (0%-3%), protein 34 g/L (42-74 g/L), and glucose 3.0 mmol/L (3.3-5.8
mmol/L). Magnetic resonance imaging of the brain showed diffuse white
matter lesions scattered in the subcortical and deep white matter over
both cerebral hemispheres and periventricular region, most prominent in
the left parietal lobe and frontoparietal regions, and subtle
hyperintense lesions in bilateral dentate nucleus (Figure, panel A). No
meningeal enhancement was noted.

Because of eosinophilic meningoencephalitis, thorough analyses were
conducted for immunologic and infectious etiologies. The family
confirmed the presence of numerous raccoons in their backyard, which
raised a concern for Baylisascaris encephalitis, and samples of
cerebrospinal fluid and serum were sent to Purdue University (West
Lafayette, IN, USA) for serologic testing. On the basis of clinical
findings, the child was given albendazole 200 mg orally 3x/day and
prednisone 25 mg orally for 4 weeks. Results of ELISA were positive for
B. procyonis from serum (optical density = 0.744; cutoff 0.250) but
negative from cerebrospinal fluid. B. procyonis-specific protein bands
were seen on Western blotting (9). The parents reported that the child
had no access to the backyard, but they and their dog often moved
between the backyard and the house. Environmental sampling was conducted
in conjunction with the public health department. Thirty samples were
taken from the patient's home and yard. A sample of raccoon feces
taken from a garbage bag from the porch of the house contained
embryonated B. procyonis eggs (Figure, panel B). No eggs were identified
in the dog. Nine months after the initial hospitalization, the child had
substantial physical and motor delays, was legally blind in both eyes,
and had epilepsy.

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To our knowledge, this is the second case of Baylisascaris
encephalitis identified in Canada. Both cases are noteworthy for
profound neurologic impairment. Similar to cases reported from the
United States, the case reported here highlights the dangers of
peridomestic raccoons, which are becoming increasingly common in both
countries. Although the classical risk factors for pica/ geophagia or
developmental delay were not reported by the patient's parents, he
could have become infected only through ingestion of infective eggs,
from an as-yet-undetermined location, object, or source. The case
reported here illustrates the need for a collaborative approach in
unusual cases; we included clinicians and public health and laboratory
specialists in the workup of this case. We found a strong correlation
between the serologic findings, the child's clinical signs, other
clinical information (e.g., eosinophilia, magnetic resonance imaging
findings), the age of the child, and the recovery of embryonated B.
procyonis eggs from his environment. We postulate that he became
infected by ingesting raccoon feces/infective eggs unintentionally
brought into the home or through exposure in adjacent structures, such
as the porch. Although no eggs were identified in the dog, several
reports have documented intestinal infection of domestic dogs with B.
procyonis, albeit at a prevalence thousands of times lower than that in
raccoons (3; J. Yang, unpub. data). That the dog served as a vector
after being exposed to raccoon feces and infective eggs is far less
likely. A recent report from the Centers for Disease Control and
Prevention suggests possible transmission from pet kinkajous (10). We
speculate that more common domestic pets also might serve as possible
reservoirs for and sources of infection.

Acknowledgments

We thank the clinical laboratory staff and the public health
departments for expert assistance and Sriveny Dangoudoubiyam for
performing the serology.